Catálogo de publicaciones - revistas

<jats:p> Advances in membrane technologies that combine greatly improved carbon dioxide (CO <jats:sub>2</jats:sub> ) separation efficacy with low costs, facile fabrication, feasible upscaling, and mechanical robustness are needed to help mitigate global climate change. We introduce a hybrid-integrated membrane strategy wherein a high-permeability thin film is chemically functionalized with a patchy CO <jats:sub>2</jats:sub> -philic grafted chain surface layer. A high-solubility mechanism enriches the concentration of CO <jats:sub>2</jats:sub> in the surface layer hydrated by water vapor naturally present in target gas streams, followed by fast CO <jats:sub>2</jats:sub> transport through a highly permeable (but low-selectivity) polymer substrate. Analytical methods confirm the existence of an amine surface layer. Integrated multilayer membranes prepared in this way are not diffusion limited and retain much of their high CO <jats:sub>2</jats:sub> permeability, and their CO <jats:sub>2</jats:sub> selectivity is concurrently increased in some cases by more than ~150-fold. </jats:p>

<jats:p> Many human abilities rely on cognitive algorithms discovered by previous generations. Cultural accumulation of innovative algorithms is hard to explain because complex concepts are difficult to pass on. We found that selective social learning preserved rare discoveries of exceptional algorithms in a large experimental simulation of cultural evolution. Participants ( <jats:italic>N</jats:italic> = 3450) faced a difficult sequential decision problem (sorting an unknown sequence of numbers) and transmitted solutions across 12 generations in 20 populations. Several known sorting algorithms were discovered. Complex algorithms persisted when participants could choose who to learn from but frequently became extinct in populations lacking this selection process, converging on highly transmissible lower-performance algorithms. These results provide experimental evidence for hypothesized links between sociality and cognitive function in humans. </jats:p>

<jats:p>Adoptive cell therapy using engineered T cell receptors (TCRs) is a promising approach for targeting cancer antigens, but tumor-reactive TCRs are often weakly responsive to their target ligands, peptide–major histocompatibility complexes (pMHCs). Affinity-matured TCRs can enhance the efficacy of TCR–T cell therapy but can also cross-react with off-target antigens, resulting in organ immunopathology. We developed an alternative strategy to isolate TCR mutants that exhibited high activation signals coupled with low-affinity pMHC binding through the acquisition of catch bonds. Engineered analogs of a tumor antigen MAGE-A3–specific TCR maintained physiological affinities while exhibiting enhanced target killing potency and undetectable cross-reactivity, compared with a high-affinity clinically tested TCR that exhibited lethal cross-reactivity with a cardiac antigen. Catch bond engineering is a biophysically based strategy to tune high-sensitivity TCRs for T cell therapy with reduced potential for adverse cross-reactivity.</jats:p>

<jats:p>The human immune system displays substantial variation between individuals, leading to differences in susceptibility to autoimmune disease. We present single-cell RNA sequencing (scRNA-seq) data from 1,267,758 peripheral blood mononuclear cells from 982 healthy human subjects. For 14 cell types, we identified 26,597 independent cis-expression quantitative trait loci (eQTLs) and 990 trans-eQTLs, with most showing cell type–specific effects on gene expression. We subsequently show how eQTLs have dynamic allelic effects in B cells that are transitioning from naïve to memory states and demonstrate how commonly segregating alleles lead to interindividual variation in immune function. Finally, using a Mendelian randomization approach, we identify the causal route by which 305 risk loci contribute to autoimmune disease at the cellular level. This work brings together genetic epidemiology with scRNA-seq to uncover drivers of interindividual variation in the immune system.</jats:p>

<jats:p> Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease. Knowledge of circulating immune cell types and states associated with SLE remains incomplete. We profiled more than 1.2 million peripheral blood mononuclear cells (162 cases, 99 controls) with multiplexed single-cell RNA sequencing (mux-seq). Cases exhibited elevated expression of type 1 interferon–stimulated genes (ISGs) in monocytes, reduction of naïve CD4 <jats:sup>+</jats:sup> T cells that correlated with monocyte ISG expression, and expansion of repertoire-restricted cytotoxic <jats:italic>GZMH</jats:italic> <jats:sup>+</jats:sup> CD8 <jats:sup>+</jats:sup> T cells. Cell type–specific expression features predicted case-control status and stratified patients into two molecular subtypes. We integrated dense genotyping data to map cell type–specific cis–expression quantitative trait loci and to link SLE-associated variants to cell type–specific expression. These results demonstrate mux-seq as a systematic approach to characterize cellular composition, identify transcriptional signatures, and annotate genetic variants associated with SLE. </jats:p>

<jats:p> We established a genome-wide compendium of somatic mutation events in 3949 whole cancer genomes representing 19 tumor types. Protein-coding events captured well-established drivers. Noncoding events near tissue-specific genes, such as <jats:italic>ALB</jats:italic> in the liver or <jats:italic>KLK3</jats:italic> in the prostate, characterized localized passenger mutation patterns and may reflect tumor-cell-of-origin imprinting. Noncoding events in regulatory promoter and enhancer regions frequently involved cancer-relevant genes such as <jats:italic>BCL6</jats:italic> , <jats:italic>FGFR2</jats:italic> , <jats:italic>RAD51B</jats:italic> , <jats:italic>SMC6</jats:italic> , <jats:italic>TERT</jats:italic> , and <jats:italic>XBP1</jats:italic> and represent possible drivers. Unlike most noncoding regulatory events, <jats:italic>XBP1</jats:italic> mutations primarily accumulated outside the gene’s promoter, and we validated their effect on gene expression using CRISPR-interference screening and luciferase reporter assays. Broadly, our study provides a blueprint for capturing mutation events across the entire genome to guide advances in biological discovery, therapies, and diagnostics. </jats:p>

<jats:p>High-entropy nanoparticles have become a rapidly growing area of research in recent years. Because of their multielemental compositions and unique high-entropy mixing states (i.e., solid-solution) that can lead to tunable activity and enhanced stability, these nanoparticles have received notable attention for catalyst design and exploration. However, this strong potential is also accompanied by grand challenges originating from their vast compositional space and complex atomic structure, which hinder comprehensive exploration and fundamental understanding. Through a multidisciplinary view of synthesis, characterization, catalytic applications, high-throughput screening, and data-driven materials discovery, this review is dedicated to discussing the important progress of high-entropy nanoparticles and unveiling the critical needs for their future development for catalysis, energy, and sustainability applications.</jats:p>

<jats:p>Science philanthropy is experiencing a growth spurt, propelled by the newly acquired wealth of individuals and foundations, as well as a desire to address challenges such as infectious disease, fire, drought, and food and water security. Especially in the United States, this is altering the dynamics of the research ecosystem, which has been dominated by government funding since the end of World War II. This change comes with new perspectives and approaches to solving the world’s problems. And it comes with a commitment to increase equity in funding.</jats:p>